Why We Get Sick (32 page)

At the very least, we might expect the evolved regulatory mechanisms to coordinate the orgasms of men and women. But orgasms are not only uncoordinated, they are systematically sooner for men than women. This bias is one of the more unfortunate illustrations of the principle that natural selection shapes us to maximize reproduction, not satisfaction. Imagine the reproductive success of a man who tends to come to orgasm very slowly. He might please his partner, but if the sex act is interrupted or his partner has been satisfied and does not want to continue, his sperm will sometimes not get to where they will do his genes any good. The same forces shape the timing of the female sexual response. A woman who rapidly has a single orgasm may, on occasion, stop intercourse before her partner ejaculates and thus will have fewer offspring than the woman with a more leisurely sexual response.

A closer look reveals that there may be a system to adjust male sexual timing according to the particular circumstances. Premature ejaculation is common mainly in young men, especially when they are in anxiety-provoking situations. According to anthropologists who study hunter-gatherer cultures, the liaisons of young men are often illicit and would be dangerous if discovered by older men. In such circumstances, brevity of the sexual act may be especially adaptive. These ideas are mere speculation now, but they deserve consideration.

P
regnancy would seem to be the ultimate in shared goals—a refuge from conflict, perfect unity of purpose between mother and fetus. And the relationship between mother and fetus is about as intimate and mutual as any relationship can be. Nonetheless, because mother and fetus share only half their genes, there is conflict aplenty. Whatever benefits go to the fetus help all its genes. The fetus maximizes its fitness by appropriating whatever maternal resources it can use short of jeopardizing the mother’s ability to care for it in the future and her ability to raise full or half brothers and sisters (all discounted by the one half or three quarters of genes they do not have in common).

From the mother’s point of view, benefits given to the fetus help only half of her genes, so that her optimum donation to the fetus is lower than the amount that is optimal for the fetus. She is also vulnerable to injury or death from the birth of too large a baby. The fitness interests of the fetus and the mother are therefore not identical, and we can predict that the fetus will have mechanisms to manipulate the mother to provide more nutrition and that the mother will have mechanisms to resist this manipulation.

People sometimes argue that there could be no net advantage to a gene that benefits an offspring at a cost to its mother, because its early advantage would be exactly reversed by the later cost. This is not the way things work out. Suppose, in a population in which maternal and fetal interests are served equitably, a gene arises that increases fetal nutrition slightly, at a slight cost to the mother. A fetus that enjoys that advantage can avoid the cost half the time when it grows up, because only half its offspring will carry the gene. Also, even more obviously, it will pay the cost only if it is female. So the cost would be paid in only about 25 percent of the pregnancies of the next generation. There are additional complexities—which we will not go into—but such quantitative considerations led Harvard biologist David Haig to expect conflict between parent and offspring, even though the ideal contribution from the mother’s perspective may be only slightly less than the ideal for the fetus.

Unfortunately, these slight differences create major conflicts. The fetus may be striving mightily to glean an extra few percent of nutrient delivery from the mother, while the mother tries just as hard to prevent
this. When the balance of power is disrupted because one participant’s efforts are seriously impaired, medical problems arise. For example, the fetus secretes a substance,
human placental lactogen
(hPL), that ties up maternal insulin so that blood glucose levels rise and provide more glucose to the fetus. The mother counters this fetal manipulation by secreting more insulin, and this makes the fetus secrete even more hPL. This hormone is normally present in all human bodies, but in a pregnant woman it can reach a thousand times the normal concentration. As Haig points out, these raised hormone levels, like raised voices, are a sign of conflict.

If the mother happens to be deficient in her production of insulin, this can cause gestational diabetes, possibly fatal to the mother, and therefore to the glucose-greedy fetus itself. The fetus would have been well advised to curtail its secretion of hPL, but all it can do is play the odds. The average mother is thoroughly competent to produce enough insulin to avoid diabetes, even when flooded by fetal hPL.

The evolutionary theory of parent-offspring conflict was worked out many years ago by Robert Trivers, but it was only in 1993 that David Haig applied it to the workings of human pregnancy. It is also only recently that an unexpected but highly relevant genetic phenomenon came to light. Experiments, mainly with mice, have shown that the genes need not rely on the lottery of sexual reproduction to avoid the later costs of special benefits in fetal development. They may resort to
genetic imprinting
, whereby a gene is somehow conditioned by its parent either to start acting immediately or to avoid acting in the offspring. Genes from a father may be imprinted so they side with a fetus in the conflict with the mother. These same genes, when they come from a mother, may be imprinted so they have no such effect. The relevance of this to human pregnancy remains to be determined, but in mice, genes imprinted by males produce a fetal growth factor and other genes imprinted by females produce a mechanism for destroying that growth factor. Such evidence suggests that it may not be farfetched to view the womb itself as the battleground on which genes play out their interests at the expense of our health.

Aside from diabetes, another scourge of pregnancy is high blood pressure. This is called preeclampsia when it gets severe enough to damage the kidneys so that protein is lost in the urine. Haig has suggested that this too may result from conflict between the fetus and the mother. In the early stages of pregnancy, the placental cells destroy the uterine nerves and arteriolar muscles that adjust blood flow, and this
makes the mother unable to reduce the flow of blood to the placenta. If something constricts other arteries in the mother, her blood pressure will go up and more blood will therefore go to the placenta. The placenta makes several substances that can constrict arteries throughout the mother’s body. When the fetus perceives that it is receiving inadequate nutrition, the placenta releases these substances into the mother’s circulation. They can damage the mother’s tissues, but selection may have shaped a fetal mechanism that takes this risk in order to benefit itself even at the expense of the mother’s health. Data on thousands of pregnancies show that moderate increases in maternal blood pressure are associated with
lower
fetal mortality, and that women with preexisting high blood pressure have larger babies. Further support is provided by findings that preeclampsia is especially common when the blood supply to the fetus is restricted, and that the mother’s high blood pressure results from increased resistance in the arteries, not from increased pumping by the heart.

We wonder if the same mechanism may explain some adult high blood pressure. Low-birth-weight infants are especially likely to develop this condition as adults. If genes that are expressed in the fetus to make substances that increase the mother’s blood pressure continue to be active, this could cause high blood pressure later in life.

From a traditional medical perspective, these explanations for diabetes and high blood pressure in pregnancy are revolutionary, and unproven, but we suspect they may well prove correct. If so, they provide extraordinary evidence for the power of looking at life from the gene’s point of view, for the ubiquity of biological conflicts of interest, and for the practical utility of an adaptationist approach to disease.

Human chorionic gonadotropin (hCG) is another hormone made by the fetus and secreted into the mother’s bloodstream. It binds to the mother’s luteinizing hormone receptors and stimulates the continued release of progesterone from the mother’s ovaries. This hormone blocks menstruation and lets the fetus stay implanted. hCG seems to have originated in the contest between the fetus and the mother over whether the pregnancy should continue or not. Up to 78 percent of all fertilized eggs are never implanted or are aborted very early in pregnancy. The majority of these aborted embryos have chromosomal abnormalities. Mothers seem to have a mechanism that detects abnormal embryos and aborts them. This adaptation prevents continued investment in a baby that would die young or be unable to compete successfully in adult life. It is advantageous for the
mother to cut her losses as early as possible and start over, even if this means culling a few normal embryos in order to avoid the risk of nurturing an abnormal one. The fetus, by contrast, does everything it can to implant itself and to stay implanted. Producing hCG is an important early strategy for the fetus to further this goal.

It seems likely that high hCG levels are somehow detected and interpreted by mothers’ bodies as a sign of a viable fetus—if it, can make enough hCG, it is probably normal. So the embryo, to demonstrate its fitness to the mother, must now make greater amounts of hCG, levels that say as loud as they can, “I am the makings of a great baby.” It is also conceivable, as Haig points out, that these high levels of hCG are a cause of nausea and vomiting in pregnancy. Do you think this an alternative to Profet’s morning-sickness theory, summarized in
Chapter 6
? Not if you understand the distinction between proximate and ultimate causes (
Chapter 2
). The hCG effect could be part of the adaptive machinery that deters ingestion of toxins. Conversely, it may just be an incidental consequence of high hCG levels. Only a well-designed investigation can resolve this issue.

T
he large brains and small pelvic openings of humans have combined to make birth especially stressful and risky. As we noted in
Chapter 9
, it would be far better if the baby could be born through an opening in the abdominal wall, as occurs artificially in a cesarean section, but historical constraints make that impossible, and the baby must still squeeze through the pelvis. The relative immaturity and helplessness of human babies compared to those of other primates are an unavoidable cost of being small enough to be born, but the dangers nonetheless remain for both baby and mother.

Wenda Trevathan, an anthropologist at New Mexico State University, notes that while other primates go off alone to give birth, human mothers often seek companionship and support. She suggests that this may in part be explained by the unusual birth orientation of human babies. In contrast to those of other primates, human babies normally emerge facing backward, so that if the mother were to try to finish a difficult labor by pulling on the baby, she might injure it. The presence of a helper at birth greatly decreases the risk. Even in modern
times, the simple presence of a supportive woman during birth can reduce the rate of cesarean section by 66 percent and the use of forceps by 82 percent. Six weeks after birth, mothers who had a helper at birth are less anxious and breast-feed more easily than mothers who gave birth without a helper.

After the baby is born, a modern obstetrician or midwife helps extract the placenta and tries to minimize bleeding. Oxytocin is a natural hormone stimulated by nursing that constricts uterine blood vessels at birth, and injections of extra oxytocin have stopped excessive bleeding and saved thousands of lives. Doctors cannot always predict who will bleed excessively, and oxytocin administration is now part of the delivery routine. There has, however, been little research on the possibility that such routine administration of oxytocin might disrupt other mechanisms.

In some species, notably sheep, birth by cesarean section usually results in the mother not accepting the offspring as her own. A ewe will kick and butt her lamb born by cesarean section. During normal birth, pressure on her vaginal walls stimulates the release of oxytocin, which activates a brain mechanism that makes the mother bond to the first lamb she sees in the next few minutes. Administration of a dose of oxytocin enables a ewe to bond normally to a lamb delivered by cesarean section. We don’t know whether oxytocin plays a similar role in human bonding. Because human mothers seem to attach normally to cesarean babies born by cesarean section, it seems that oxytocin may not be necessary to bonding by human mothers. Need this mean it doesn’t help? Because the issue is so important, and because of the frequency of cesarean sections and the routine administration of large doses of extra oxytocin, further study of the positive and negative effects of this hormone is needed.

W
hen the baby first nurses at the mother’s breasts, they secrete not milk but colostrum, a watery liquid full of substances that protect the baby from infection. In a few days, the real milk comes in, which also contains a variety of substances that protect the baby far better than anything in infant formula. Much has been said about
the benefits of natural breast-feeding, and we will not belabor the point, except to note parenthetically how completely nonadaptive human behavior can be in the modern environment. For instance, four of Mozart’s six children died in the first three years of life—tragic but not surprising when we learn that they were fed mainly sugar water.

Many babies now spend a few extra days in the hospital because they are jaundiced. The yellow color results from high levels of bilirubin, a by-product of the breakdown of hemoglobin. At the time of birth, fetal hemoglobin, which is well suited to the intrauterine environment, is being replaced by the adult form, which is better suited to life outside the womb. If the liver gets behind in processing the great onslaught of hemoglobin derivatives, a certain amount of jaundice is both understandable and unremarkable.